Since 1989, Grand Canyon has been experiencing
an ever-increasing rate of hyponatremia. Hyponatremia means low sodium
concentration in the blood. Sometimes called water intoxication due to
the neurological symptoms, the mechanism is far more complex than simply
drinking too much water. This is not just a Grand Canyon phenomenon. Ultra
endurance events including marathons, triathlons and even the popular
“eco-challenges” are seeing an increase in incidents. Last
year, there were 30 documented cases of exertional hyponatremia, seven
of which were admitted into the icu with intracranial pressure (icp).
Although most of these occur with hikers, passengers on commercial/ private
river trips have also developed hyponatremia.
Let's look at how our bodies respond to a heat challenge situation.
Dehydration is a form of hypovolemic shock. Dehydration-volume shock is
a progressive disorder that, if unhalted, spirals downward into deeper
levels of hemodynamic and metabolic deterioration. Exertion further exacerbates
the perfusion pressure in the system. Exercise in a hot environment forces
the body to shift large amounts of fluid way from core circulation (brain,
heart, and lungs) to the skin and skeletal muscle in order to dissipate
heat. This is referred to a core-shell shift. Fluid is also lost through
secretion of sweat and from breathing. Sweat can contain as much as 90
mEq/liter of sodium. Compare that with Gatorade which contains only 10
mEq/ liter. The tank gets lower and lower, profusion pressure drops, the
hiker's performance drops, fatigue sets in, and you have the beginnings
of heat exhaustion. The body in its amazing ability to maintain equilibrium
will begin shunting blood from the Gastrointestinal (gi) tract (gut) and
other less needed areas. This results in little absorption of food and
water from the stomach and intestines—the power bar and Gatorade
just sit there. Any guess what happens next…you begin to feel nauseous
and sick to your stomach. As volume, shock continues the body will shift
from a core-shell movement to a shell-core. The long-term risk of this
is soaring core temperatures. Because the maximum rate of gastric emptying
is much less than the maximum sweat rate (1.2 verses 3.7 l/hr). Rehydration
cannot keep pace with sweat losses under those conditions. This puts you
behind the power curve. Rehydration and replacement of electrolytes lost
in sweat via oral intake may require 36 hours with occasional urination
Water intoxication is an old term for exercise induced dilutional hyponatremia
or exertional hyponatremia for short. Hyponatremia occurs when the proportion
of Total Body Water (tbw) to total sodium is excessive and a hypo-osmolar
hyponatremia develops. You can get this and still be dehydrated. How did
we get there is the question. Actually, there are several mechanisms coming
into play here. The first problem is drinking too much freewater and not
replacing lost electrolytes. The second is the spacing of hypotonic fluids
in the gut during exertion. The third problem is a syndrome of inappropriate
antidiuretic hormone (adh) response, known as siadh. All three mechanisms
can be working to together.
The Role of AIH
One compensating mechanism of the body is the release of adh (antidiuretic
hormone). It is released by the pituitary gland in response either blood
volume or changes in sodium concentration, known as osmolarity. Osmolarity
is the concentration of ions in any given solvent. A fall in blood volume
causes a release of adh—to try to get the kidney to conserve more
water and bring the volume back up. A low concentration of sodium causes
the pituitary to decrease the amount of adh and you pee out more urine.
Thus, low sodium diets help hypertension by decreasing volume.
So what happens when we begin to loss both sodium and volume? The former
tells the pituitary gland to decrease adh and the latter tells it to increase.
The result is conflicting messages, but protecting blood volume is a survival
mechanism and in the case of a hiker who is dehydrated and hyponatremic,
the pituitary will continue to release adh to hold onto water, worsening
the hyponatremia. Hopefully the brain thinks, this joker will stop hiking
and find a salt lick soon.
Why then when people are normal volume and hydrated, does adh continue
to conserve water creating a hyper-hydration and dilution of plasma sodium
ions? I do not know, but I have some theories. Many hikers at Grand Canyon
probably begin their hike in a dehydrated state due to lifestyle influences
of caffeine consumption, alcohol intake, etc. Nausea, vomiting, and fear
are also potent stimuli for excessive adh secretion. In each exercise
induced hyponatremia case I have seen, there has been at least one of
these symptoms. The fear associated with hyponatremia is so severe the
patients hyperventilate and have stated that they thought they were separating
from their body or floating away from their body and, therefore, they
were surely dying. Siadh may be more significant in the development of
acute hyponatremia than sweat loss and water consumption. Siadh may be
a phenomenon that worsens the patient's situation from mild hyponatremia
So, let me give you a summary scenario. Hikers
come into their hike dehydrated chronically. Adh is circulating. They
read in Backpacker Magazine that you need to hydrate yourself while hiking
and that these fancy sport drinks are not needed. So they drink and drink
and sweat and sweat. Sodium and water is lost through sweat and not replaced.
Adh conserves free water, causing blood sodium osmolarity to decrease.
Sodium levels continue to drop, serum osmolarity continues to drop. Hyponatremia
sets in. Bad things begin to happen. Fluids shifts from outside the cell
inside, causing swelling. Brain cells begin to swell, causing increased
intracranial pressure and bad neurological changes including headache,
confusion, staggered gait, seizures, and unconsciousness.
Let me muddy the waters. Not only will hikers or triathlon participants
experience extensional hyponatremia during their hike, but the symptoms
sometimes are delayed several hours, usually after the hike or event is
over. Remember we talked about the third spacing of fluids in the gut
because it is ischemic. This free water often sits for hours. Delayed
dilutional hyponatremia occurs when dehydration shock has occurred and
the patient probably has had severe gut ischemia with minimal water absorption
in the intestinal area. The patient now consumes a large quantity of water
or exercise drink. Add that to what was stored in the gut and you have
a high level of hypotonic fluids. You rest, your gut is no longer ischemic
and releases hypotonic fluid into the bloodstream, diluting sodium levels,
and bingo you start seizing in camp, long after the hike is over.
Approach to Patient Assessment
Physical exam will reveal normal vital signs. Temperature is normal or
low. Mental status changes are the key to assessment. Early symptoms include
general malaise, fatigue, headache and nausea. As you can see these are
very similar to heat exhaustion. That is where the assessment criteria
gets tricky. If you treat a heat exhausted patient with hydration and
rest, they will get better. If you treat a hyponatremic patient with fluids
and rest, they will get worse. Although we have never had a death a Grand
Canyon, there was a recent fatality on a army base, where a recruit in
boot camp died of cerebral and pulmonary edema after army medic mistook
his hyponatremia for severe heat exhaustion and forced fluids on him.
Because hyponatremia looks so much like heat exhaustion in its early stages
and can mimic heat stroke once the person seizures, the park rangers have
come to rely on portable blood chemical analysis in the field. These machines
will measure the level of sodium in the blood stream and give us a better
idea of what is going on. They are expensive but worth it.
Management of Exertional Induced Hyponatremia
• Place patients in a sitting up position. Lying down could increase
intracranial pressure and accelerate cerebral edema. If the patient is
p or lower on the avpu (Alert, Verbal, Pain, Unconscious) scale, place
them in a left lateral position. Watch for vomiting. It should be an anticipated
problem. Patients are prone to aspiration.
• Increase sodium levels slowly.
• Keep the patient calm. Fear along with a gloom and doom attitude
stems from a detached, almost floating sensation these patients experience
allowing an onset of anxiety induced hyperventilation syndrome to ensue.
Anxiety induced hyperventilation should be discouraged.
• Watch for seizures. If patient seizes, airway management is a
top priority. Once the patient seizes, they will remain aloc.
So what is the take home message…Prevention is the key.
Stay hydrated and nourished. Once hiking, keep a steady intake of water
or electrolyte replacement drink and eat. I cannot emphasis this enough.
Sport physiologists assume people are eating and therefore do not need
commercial electrolyte replacement. The truth of the matter is that people
don't eat when they are hot, and they don't eat once they
become dehydrated and sick. Gatorade, which contains the highest sodium
concentration, doesn't even come close to the 35 mEq/liter/ hour
needed to replace lost salt through sweat. What kind of food, my personal
preference is salty snack food. This is not a time for power bars. Leave
the health food behind. Junk food is great. Stock up. The rangers now
routinely give out saltine crackers, pretzels and cheezits. Stay ahead
of the sodium curve!
Sherrie Collins, Chief,
Branch of Emergency Services